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Oximes in Organophosphorus Poisoning IJCCM October-December 2003 Vol 7 Issue 4 Indian J Crit Care Med July-September 2005 Vol 9 Issue 3 Review Article Oximes in organophosphorus poisoning M. A. Cherian,1 Roshini C,2 J. V. Peter,3 A. M. Cherian4 Acute organic insecticide poisoning is a major health problem all over the world, particularly in the develop­ ing countries, where organophosphates (OPs) are the most common suicidal poisons with high morbidity and mortality and account for a large proportion of patients admitted to intensive care units. Other insecti­ Abstract cides less commonly used are organocarbamates, organochlorides, and pyrethroids, which are less toxic and are associated with less morbidity and mortality. Patients with poisoning present with a wide spectrum of gastrointestinal, neurological, and cardiac manifestations. A strong clinical suspicion is necessary to make an early diagnosis and to start appropriate therapy. Treatment is primarily supportive and includes decontamination, anticholinergics, protection of the airway, and cardiac and respiratory support. The use of oximes has been controversial and may be associated with higher mortality owing to a higher incidence of type-II paralysis. They may have other toxic side effects. This paper reviews the literature on OP poisoning. Key Words: Anticholinergics, Manifestations, Organophosphate, Oximes, Poisoning Introduction tries.[2] There has been a change in the type of agents Organophosphate (OP) compounds have been used used for suicide attempts, with OP poisoning being seen worldwide for pest control for over 100 years. They are more and more frequently as compared with phenobar­ the insecticides of choice in the agricultural world and bitone, diazepam, hypnotics, and antidepressants a cou­ are the most common cause of poisoning among the ple of decades ago. In the Christian Medical College organic insecticides. They are common agents of sui- (CMC) and Hospital, Vellore, India, OP poisoning ac­ cidal and accidental poisoning, as a result of their ready counted for 12% of all admissions to the medical inten­ availability and easy accessibility. Several hundred peo- sive care unit (ICU) and 29% of all poisoning in the early ple around the world die each year from OP poisoning, 1990s[3] and now accounts for over 70% of all poisonings. especially in developing countries.[1] Recently, there has In another center 89.75% of patients admitted with poi­ been a renewed interest in OP compounds as these are soning were owing to OP.[4] OP compounds are com­ agents which might be used as chemical weapons. mon suicidal agents in Pakistan,[5] Sri Lanka,[6] and the other Asian and South East Asian countries. The WHO estimates that three million cases of poi­ soning occur worldwide, mostly in the developing coun- The OP compounds are popular insecticides because of their effectiveness and nonpersistence in the envi- From: ronment owing to their unstable chemical nature. They 1Merit Care/UND Program, MeritCare Medical Group, Fargo, ND 58122,USA. do not persist in the body or environment as do 2Launceston General Hospital, Launceston, Tasmania, Australia. 3The Queen Elizabeth Hospital, Adelaide, S.A 5011, Australia. organochlorides and have become the insecticide group 4Department of Medicine, TMM Hospital, Tiruvalla 689101, India. of choice replacing DDT, an organochloride compound.[7] Correspondence: Dr. A. M. Cherian, TMM Hospital, Tiruvalla 689101, Kerala, India. E-mail: [email protected] OPs are common household insecticides used exten- Free full text available from www.ijccm.org 155 Indian J Crit Care Med July-September 2005 Vol 9 Issue 3 IJCCM October-December 2003 Vol 7 Issue 4 sively by agricultural communities. Seasonal variations Most OPs are well absorbed from skin, oral mucous in water availability keep these communities in financial membranes, conjunctival mucous membrane, and debt, driving farmers to suicide by ingestion of agricul­ gastrointestinal and respiratory routes. Subsequently, tural pesticides that are sold directly over the counter most OP compounds are hydrolyzed by enzymes, the A and have inadequate regulations controlling their use esterases or paroxonases, which are not inhibited by and storage. Early and correct diagnosis and treatment OP compounds. These enzymes are found in the plasma may be life-saving in OP poisoning. It is important to and in the hepatic endoplasmic reticulum and split the treat cases in hospitals with respiratory support facili­ anhydride, P–F, P–CN, or ester bonds.[10] The metabolic ties to reduce the morbidity and mortality. products are then excreted in the urine. OP compounds that bind to acetylcholinesterase block the conversion Historical Perspective of acetylcholine to its degradation products, namely, The first OP compound synthesized in 1854 was acetic acid and choline. This leads to a build-up of ex­ tetraethyl pyrophosphate (TEPP). It came into use in cessive acetylcholine at synapses, which is the primary Germany during World War II as an agricultural pesti­ cause of most of the toxic effects of OP compounds. cide substitute for nicotine and for possible use as a nerve gas in chemical warfare. It is also the most toxic Pathophysiology of OP Poisoning of the OP insecticides.[8] Parathion, an organic deriva­ Acetylcholine is the neurotransmitter released by the tive of phosphoric acid, was synthesized shortly after terminal nerve endings of all postganglionic World War II. Because it has to be converted to paraoxon parasympathetic nerves and in both sympathetic and by substitution of oxygen for sulfur to be physiologically parasympathetic ganglia. It is also released at the skel­ active, symptoms of parathion intoxication are often de­ etal myoneural junctions and serves as a neurotrans­ layed for 6–24 h. There have been numerous OP com­ mitter in the central nervous system.[11] Acetylcholineste­ pounds synthesized over the years and over a hundred rase is present in two forms: true cholinesterase which compounds are currently available under different brand is found primarily in the nervous tissue and erythrocytes names, making identification difficult in a given patient, and pseudocholinesterase which is found in the serum unless the container is brought in by the patient’s rela­ and liver.[9] OPs bind to the active serine residue of acetyl tive. Of the OP group, Parathion is the most common cholinesterase irreversibly and convert the enzyme into cause of human poisoning and fatality.[9] Table 1: Factors determining the onset, duration, and Pharmacology intensity of OP poisoning The OP compounds are classified in many ways; one Nature of compound Remarks [9] Water-soluble Acute and shorter duration of based on clinical toxicity is as follows: symptoms, e.g., TEPP 1. Agricultural insecticides (high toxicity), for example, Lipid-soluble Delayed and more sustained TEPP, parathion, phorate, mevinphos, and disulfoton. effect, e.g., chlorfenthion Nature of binding 2. Animal insecticides (intermediate toxicity), for exam­ Reversible Short-lived effects ple, coumaphos, chlorpyrifos, trichlorfon, and ronnel. Irreversible Persistent effects, e.g., parathion Mode of action 3. Household use or use in golf courses (low toxicity) , Direct agent Direct acetyl cholinesterase for example, diazinon, malathion, dichlorvos, and inhibition, e.g., sarin Indirect agent Needs to be converted to active acephate. metabolite, e.g., parathion Route/degree of exposure Cutaneous Chronic toxicity OPs may also be classified according to their pharma­ Oral/GIT Acute symptoms cokinetics as given below. Inhaled May be acute or chronic depending on poison load Relative toxicity of the compound Pharmacokinetics Low The onset, intensity, and duration of pharmacological Intermediate High effects that occur after poisoning are determined largely Rate of metabolic degradation by the factors listed in Table 1. Malathion 156 IJCCM October-December 2003 Vol 7 Issue 4 Indian J Crit Care Med July-September 2005 Vol 9 Issue 3 an inactive protein complex, resulting in the accumula­ Neurological Manifestations in OP tion of acetylcholine at the receptors, leading to Poisoning overstimulation and subsequent disruption of nerve im­ Neurological manifestations are the most important pulse transmission in both the peripheral and central sequelae of OP poisoning as a large number of patients nervous systems. with acute OP poisoning develop neuromuscular weak­ ness requiring prolonged ventilation. Three types of pa­ Etiology of OP Poisoning ralyses are recognized based on the time of occurrence OP poisoning results either from suicidal or accidental and differ in their pathophysiology. poisoning or from occupational exposure such as farm­ ing. A large proportion (68%) of patients presented to Type-I Paralysis or Acute Paralysis the ICU following an acute suicide attempt.[6,8] Most pa­ Type-I paralysis occurs with the initial cholinergic cri­ tients are young (less than 30 years) with a male pre­ sis. This is postulated to be owing to the persistent de­ ponderance.[8,12] Occupational and accidental poisoning polarization at the neuromuscular junction resulting from occur less commonly in India.[8] blockade of acetylcholinesterase, and usually develops within 24–48 h. Features include muscle fasciculations, Clinical Features of Poisoning cramps, twitching, and weakness. These manifestations Clinical features of acute poisoning occur within 24 h respond to atropine,[14] although it may not fully block of ingestion of the OP compound. These can be broadly the nicotinic effects. Muscle weakness
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